scholarly journals Effect of Huangqin decoction on regulating intestinal flora in colitis mice characterized as inhibition of the NOD2-dependent pathway

2021 ◽  
Vol 60 (1) ◽  
pp. 108-118
Author(s):  
Shaowei Huang ◽  
Jinrong He ◽  
Yanping Chen ◽  
Xiaojing Wang ◽  
Yanyang Li ◽  
...  
2020 ◽  
Author(s):  
Shaowei Huang ◽  
Jinrong He ◽  
Yanping Chen ◽  
Xiaojing Wang ◽  
Yanyang Li ◽  
...  

Abstract Background: Dysfunction of the intestinal flora is an important factor in the occurrence and development of ulcerative colitis (UC). Chinese herb Huangqin decoction (HQD) can regulate intestinal flora in UC mice, yet its specific mechanism remains unclear. Our study aimed to clarify the mechanism of HQD in regulating intestinal flora of UC mice.Methods: 3%DSS - induced colitis mice were used to explore the pharmacodynamics of HQD. Colonic bacterial infiltration and the changes of intestinal flora were detected by FISH and 16SrDNA. Expression of RegⅢγ and PRRs (NOD2, TLR5, TLR4) were detected by FCM and WB, respectively. In addition, WB, SqPCR, or IHC were used for the expression of Nod2, MyD88, Rip2, and NF-κB p65 in colon. Cytokines were determined by ELISA.Results: HQD significantly restored the weight, the colonic length, and peripheral blood cell counts of colitis mice; reduced the DAI score and the histological score. 16SrDNA identification showed HQD regulated the balance of intestinal flora. Moreover, the expression of RegⅢγ was suppressed and colonic bacterial infiltration was prevented by HQD. Furthermore, the results of WB showed expression of NOD2 and TLR4 was inhibited by HQD, especially NOD2. And the data of WB, SqPCR and IHC explained that the NOD2-dependent pathway was inhibited by HQD.Conclusions: Our results reveal the mechanism of HQD(1g/kg) in regulating the intestinal flora of colitis mice, which may be closely characterized as the inhibition of the activation of Pattern Recognition Receptors (PRRs), especially NOD2.


1996 ◽  
Vol 76 (05) ◽  
pp. 774-779 ◽  
Author(s):  
John T Brandt ◽  
Carmen J Julius ◽  
Jeanne M Osborne ◽  
Clark L Anderson

SummaryImmune-mediated platelet activation is emerging as an important pathogenic mechanism of thrombosis. In vitro studies have suggested two distinct pathways for immune-mediated platelet activation; one involving clustering of platelet FcyRIIa, the other involving platelet-associated complement activation. HLA-related antibodies have been shown to cause platelet aggregation, but the mechanism has not been clarified. We evaluated the mechanism of platelet aggregation induced by HLA-related antibodies from nine patients. Antibody to platelet FcyRIIa failed to block platelet aggregation with 8/9 samples, indicating that engagement of platelet FcyRIIa is not necessary for the platelet aggregation induced by HLA-related antibodies. In contrast, platelet aggregation was blocked by antibodies to human C8 (5/7) or C9 (7/7). F(ab’)2 fragments of patient IgG failed to induce platelet activation although they bound to HLA antigen on platelets. Intact patient IgG failed to aggregate washed platelets unless aged serum was added. The activating IgG could be adsorbed by incubation with lymphocytes and eluted from the lymphocytes. These results indicate that complement activation is involved in the aggregation response to HLA-related antibodies. This is the first demonstration of complement-mediated platelet aggregation by clinical samples. Five of the patients developed thrombocytopenia in relationship to blood transfusion and two patients developed acute thromboembolic disease, suggesting that these antibodies and the complement-dependent pathway of platelet aggregation may be of clinical significance.


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